Damage accumulation in long-living macromolecules (especially extracellular matrix (ECM) proteins, nuclear pore complex (NPC) proteins, and histones) is a missing hallmark of aging. Stochastic non-enzymatic modifications of ECM trigger cellular senescence as well as many other hallmarks of aging affect organ barriers integrity and drive tissue fibrosis. The importance of it for aging makes it a key target for interventions. The most promising of them can be AGE inhibitors (chelators, O-acetyl group or transglycating activity compounds, amadorins and amadoriases), glucosepane breakers, stimulators of elastogenesis, and RAGE antagonists.

中文翻译：

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长寿命大分子的随机非酶修饰-缺少衰老的标志。

长寿大分子（尤其是细胞外基质（ECM）蛋白，核孔复合物（NPC）蛋白和组蛋白）中的损伤积累是衰老的缺失标志。ECM的随机非酶修饰会触发细胞衰老，以及许多其他衰老标志会影响器官屏障的完整性并驱动组织纤维化。它对衰老的重要性使其成为干预的主要目标。它们中最有前途的可以是AGE抑制剂（螯合剂，O-乙酰基或糖基转移活性化合物，阿马多林和金刚烷酶），破糖片，弹性形成刺激物和RAGE拮抗剂。